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Case Study
Successful repair of mesenteric ischemia in acute type A aortic dissection
Asian Cardiovascular & Thoracic Annals 0(0) 1–3 ß The Author(s) 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0218492314549330 aan.sagepub.com
Yoichi Hisata1, Ichiro Matsumaru2, Shogo Yokose1 and Shiro Hazama1
Abstract A 64-year-old man with acute type A aortic dissection had superior mesenteric artery occlusion and marked metabolic acidosis. By an emergency laparotomy, bypass grafting from the left external iliac artery to the superior mesenteric artery was performed with great saphenous vein. After deep sedation and antihypertensive management in the intensive care unit, the acidosis resolved, and central repair was carried out. At 10 months postoperatively, his course has been uneventful without mesenteric complications.
Keywords Aneurysm, dissecting, aortic aneurysm, ischemia, mesenteric vascular occlusion, regional blood flow, time factors
Introduction Surgical outcomes of acute type A aortic dissection have improved. However, mortality rates from malperfusion, especially mesenteric ischemia, remain high, and outcomes are poor.1–7 Controversy persists concerning therapeutic strategies including whether central repair is necessary prior to other strategies. We describe a case of mesenteric ischemia caused by acute type A aortic dissection, with a favorable outcome due to first performing bypass grafting from the left external iliac artery (EIA) to the superior mesenteric artery (SMA), followed by central repair.
Case report A 64-year-old man was brought to the emergency department with sudden chest and back pain. Computed tomography revealed acute type A aortic dissection with a patent false lumen. The celiac artery branched from the false lumen and was patent without dissection. The SMA was dissected at its origin with an approximately 1-cm thrombotic occlusion in the middle section (Figure 1). Although contrast enhancement of the intestine was relatively maintained, some image portions were unclear. The stool was mucous and bloody. Laboratory data showed a white blood cell increase to 19,470/mL, while lactate dehydrogenase
was only mildly increased to 314 UL 1. Marked metabolic acidosis was indicated by pH 7.12, base excess 15 mmolL 1, and lactate 100 mgdL 1 on blood gas analysis. Surgery was started by a laparotomy. Although the small intestine was mottled with ischemic lesions, intestinal resection was avoided because none had progressed to necrosis. Left EIA-SMA bypass grafting was performed with great saphenous vein. The patient received deep sedation and antihypertensive therapy, continuous hemodiafiltration, and prostaglandin administration in the intensive care unit. Although creatine kinase rose markedly to 4448 UL 1 the following day, it gradually decreased thereafter, and the acidosis resolved. Three days later, cardiopulmonary bypass was undertaken with concomitant antegrade selective cerebral perfusion, and hemiarch replacement with brachiocephalic artery 1 Division of Cardiovascular Surgery, Sasebo City General Hospital, Nagasaki, Japan 2 Division of Cardiovascular Surgery, Nagasaki University Hospital, Nagasaki, Japan
Corresponding author: Yoichi Hisata, MD, Division of Cardiovascular Surgery, Sasebo City General Hospital, 9-3 Hirasemachi, Sasebo City, Nagasaki 857–8511, Japan. Email: [email protected]
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Figure 1. Computed tomography showing (a, b) acute type A aortic dissection with a patent false lumen, (c) the superior mesenteric artery dissected at its origin, and (d) thrombotic occlusion (gray arrow) in the superior mesenteric artery.
reconstruction was performed during circulatory arrest after lowering the rectal temperature to 27 C. The postoperative course was favorable, and computed tomography revealed no problems at the central repair and left EIA-SMA bypass graft sites (Figure 2). At 10 months postoperatively, the patient was being managed as an outpatient.
Discussion Although surgical outcomes of acute type A aortic dissection have improved, mortality is still high in cases with concomitant malperfusion, especially mesenteric ischemia. Acute type A aortic dissection is reportedly complicated by malperfusion in 20%–50% of cases and by mesenteric ischemia in approximately 5%.1–7 It remains controversial whether central repair or mesenteric revascularization should be prioritized in treating acute type A aortic dissection complicated by mesenteric ischemia. Central repair can prevent a sudden crisis due to cardiac tamponade or rupture and also resolve impaired perfusion in branches by rapidly increasing blood flow in the true lumen. Fann and colleagues1 reported a 64% operative mortality rate in patients with peripheral vascular ischemia who underwent central repair for acute distal dissection. However, their mortality rate exceeded 80% in cases requiring
Figure 2. Three-dimensional computed tomography after ascending aorta repair with the brachiocephalic artery reconstructed. The saphenous vein bypass graft is clearly patent (red arrow).
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laparotomy due to mesenteric ischemia. Girardi and colleagues2 reported that antegrade flow into the true lumen could be reestablished within 3 h after the diagnosis of acute type A aortic dissection, and that the mortality of patients with malperfusion was 33%. We agree with their opinion that the time interval between the onset of dissection with malperfusion and definitive treatment is important, and that a delay in treatment can worsen the degree of ischemic end-organ dysfunction. However, we consider that mesenteric revascularization would be required before central repair in cases with thrombus formation in the branching blood vessels of the abdomen and significant preoperative metabolic acidosis, as in the present case, because there is not enough time to prevent intestinal ischemia from causing necrosis. The basis for mesenteric revascularization is that, in a complex subset of patients, blood flow to the ischemic territory should be rapidly reestablished while minimizing the risk of fatal ascending aortic rupture, and surgical outcomes become acceptable once the inflammatory cascade subsides.3 We also consider the mortality risk from severe visceral malperfusion to outweigh the rupture risk. Surgeons at the University of Michigan developed a strategy of restoring end-organ perfusion preoperatively in all such patients, achieving an early mortality rate of 40.5% in patients with mesenteric malperfusion.4,5 They concluded that immediate reperfusion, stabilization, and planned operative repair for acute type A aortic dissection with malperfusion still carries significant risks of early and late mortality. In our case, we selected a laparotomy, which allowed observation of the intestine and intestinal resection if necessary, and extraanatomic bypass using the EIA, which was free from dissection and could be rapidly exposed, for inflow. Given the small diameter of the peripheral SMA and the possibility of infection, great
saphenous vein was used instead of a prosthetic graft. When strict intensive care unit management after bypass grafting suppresses the inflammatory cascade, central repair is an effective approach. Funding This research received no specific grant from any funding agency in the public, commerical, or not-for-profit sectors.
Conflict of interest statement None declared.
References 1. Fann JI, Sarris GE, Mitchell RS, et al. Treatment of patients with aortic dissection presenting with peripheral vascular complications. Ann Surg 1990; 212: 705–713. 2. Girardi LN, Krieger KH, Lee LY, Mack CA, Tortolani AJ and Isom OW. Management strategies for type A dissection complicated by peripheral vascular malperfusion. Ann Thorac Surg 2004; 77: 1309–1314. 3. Lauterbach SR, Cambria RP, Brewster DC, et al. Contemporary management of aortic branch compromise resulting from acute aortic dissection. J Vasc Surg 2001; 33: 1185–1192. 4. Deeb GM, Williams DM, Bolling SF, et al. Surgical delay for acute type A dissection with malperfusion. Ann Thorac Surg 1997; 64: 1669–1675. 5. Patel HJ, Williams DM, Dasika NL, et al. Operative delay for peripheral malperfusion syndrome in acute type A aortic dissection: a long-term analysis. J Thorac Cardiovasc Surg 2008; 135: 1288–1296. 6. Yagdi T, Atay Y, Engin C, et al. Impact of organ malperfusion on mortality and morbidity in acute type A aortic dissections. J Card Surg 2006; 21: 363–369. 7. Hagan PG, Nienaber CA, Isselbacher EM, et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA 2000; 283: 897–903.
Downloaded from aan.sagepub.com by guest on November 15, 2015
(AAN)
[1–3] [PREPRINTER stage]
Case Study
Successful repair of mesenteric ischemia in acute type A aortic dissection
Asian Cardiovascular & Thoracic Annals 0(0) 1–3 ß The Author(s) 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0218492314549330 aan.sagepub.com
Yoichi Hisata1, Ichiro Matsumaru2, Shogo Yokose1 and Shiro Hazama1
Abstract A 64-year-old man with acute type A aortic dissection had superior mesenteric artery occlusion and marked metabolic acidosis. By an emergency laparotomy, bypass grafting from the left external iliac artery to the superior mesenteric artery was performed with great saphenous vein. After deep sedation and antihypertensive management in the intensive care unit, the acidosis resolved, and central repair was carried out. At 10 months postoperatively, his course has been uneventful without mesenteric complications.
Keywords Aneurysm, dissecting, aortic aneurysm, ischemia, mesenteric vascular occlusion, regional blood flow, time factors
Introduction Surgical outcomes of acute type A aortic dissection have improved. However, mortality rates from malperfusion, especially mesenteric ischemia, remain high, and outcomes are poor.1–7 Controversy persists concerning therapeutic strategies including whether central repair is necessary prior to other strategies. We describe a case of mesenteric ischemia caused by acute type A aortic dissection, with a favorable outcome due to first performing bypass grafting from the left external iliac artery (EIA) to the superior mesenteric artery (SMA), followed by central repair.
Case report A 64-year-old man was brought to the emergency department with sudden chest and back pain. Computed tomography revealed acute type A aortic dissection with a patent false lumen. The celiac artery branched from the false lumen and was patent without dissection. The SMA was dissected at its origin with an approximately 1-cm thrombotic occlusion in the middle section (Figure 1). Although contrast enhancement of the intestine was relatively maintained, some image portions were unclear. The stool was mucous and bloody. Laboratory data showed a white blood cell increase to 19,470/mL, while lactate dehydrogenase
was only mildly increased to 314 UL 1. Marked metabolic acidosis was indicated by pH 7.12, base excess 15 mmolL 1, and lactate 100 mgdL 1 on blood gas analysis. Surgery was started by a laparotomy. Although the small intestine was mottled with ischemic lesions, intestinal resection was avoided because none had progressed to necrosis. Left EIA-SMA bypass grafting was performed with great saphenous vein. The patient received deep sedation and antihypertensive therapy, continuous hemodiafiltration, and prostaglandin administration in the intensive care unit. Although creatine kinase rose markedly to 4448 UL 1 the following day, it gradually decreased thereafter, and the acidosis resolved. Three days later, cardiopulmonary bypass was undertaken with concomitant antegrade selective cerebral perfusion, and hemiarch replacement with brachiocephalic artery 1 Division of Cardiovascular Surgery, Sasebo City General Hospital, Nagasaki, Japan 2 Division of Cardiovascular Surgery, Nagasaki University Hospital, Nagasaki, Japan
Corresponding author: Yoichi Hisata, MD, Division of Cardiovascular Surgery, Sasebo City General Hospital, 9-3 Hirasemachi, Sasebo City, Nagasaki 857–8511, Japan. Email: [email protected]
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Asian Cardiovascular & Thoracic Annals 0(0)
Figure 1. Computed tomography showing (a, b) acute type A aortic dissection with a patent false lumen, (c) the superior mesenteric artery dissected at its origin, and (d) thrombotic occlusion (gray arrow) in the superior mesenteric artery.
reconstruction was performed during circulatory arrest after lowering the rectal temperature to 27 C. The postoperative course was favorable, and computed tomography revealed no problems at the central repair and left EIA-SMA bypass graft sites (Figure 2). At 10 months postoperatively, the patient was being managed as an outpatient.
Discussion Although surgical outcomes of acute type A aortic dissection have improved, mortality is still high in cases with concomitant malperfusion, especially mesenteric ischemia. Acute type A aortic dissection is reportedly complicated by malperfusion in 20%–50% of cases and by mesenteric ischemia in approximately 5%.1–7 It remains controversial whether central repair or mesenteric revascularization should be prioritized in treating acute type A aortic dissection complicated by mesenteric ischemia. Central repair can prevent a sudden crisis due to cardiac tamponade or rupture and also resolve impaired perfusion in branches by rapidly increasing blood flow in the true lumen. Fann and colleagues1 reported a 64% operative mortality rate in patients with peripheral vascular ischemia who underwent central repair for acute distal dissection. However, their mortality rate exceeded 80% in cases requiring
Figure 2. Three-dimensional computed tomography after ascending aorta repair with the brachiocephalic artery reconstructed. The saphenous vein bypass graft is clearly patent (red arrow).
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laparotomy due to mesenteric ischemia. Girardi and colleagues2 reported that antegrade flow into the true lumen could be reestablished within 3 h after the diagnosis of acute type A aortic dissection, and that the mortality of patients with malperfusion was 33%. We agree with their opinion that the time interval between the onset of dissection with malperfusion and definitive treatment is important, and that a delay in treatment can worsen the degree of ischemic end-organ dysfunction. However, we consider that mesenteric revascularization would be required before central repair in cases with thrombus formation in the branching blood vessels of the abdomen and significant preoperative metabolic acidosis, as in the present case, because there is not enough time to prevent intestinal ischemia from causing necrosis. The basis for mesenteric revascularization is that, in a complex subset of patients, blood flow to the ischemic territory should be rapidly reestablished while minimizing the risk of fatal ascending aortic rupture, and surgical outcomes become acceptable once the inflammatory cascade subsides.3 We also consider the mortality risk from severe visceral malperfusion to outweigh the rupture risk. Surgeons at the University of Michigan developed a strategy of restoring end-organ perfusion preoperatively in all such patients, achieving an early mortality rate of 40.5% in patients with mesenteric malperfusion.4,5 They concluded that immediate reperfusion, stabilization, and planned operative repair for acute type A aortic dissection with malperfusion still carries significant risks of early and late mortality. In our case, we selected a laparotomy, which allowed observation of the intestine and intestinal resection if necessary, and extraanatomic bypass using the EIA, which was free from dissection and could be rapidly exposed, for inflow. Given the small diameter of the peripheral SMA and the possibility of infection, great
saphenous vein was used instead of a prosthetic graft. When strict intensive care unit management after bypass grafting suppresses the inflammatory cascade, central repair is an effective approach. Funding This research received no specific grant from any funding agency in the public, commerical, or not-for-profit sectors.
Conflict of interest statement None declared.
References 1. Fann JI, Sarris GE, Mitchell RS, et al. Treatment of patients with aortic dissection presenting with peripheral vascular complications. Ann Surg 1990; 212: 705–713. 2. Girardi LN, Krieger KH, Lee LY, Mack CA, Tortolani AJ and Isom OW. Management strategies for type A dissection complicated by peripheral vascular malperfusion. Ann Thorac Surg 2004; 77: 1309–1314. 3. Lauterbach SR, Cambria RP, Brewster DC, et al. Contemporary management of aortic branch compromise resulting from acute aortic dissection. J Vasc Surg 2001; 33: 1185–1192. 4. Deeb GM, Williams DM, Bolling SF, et al. Surgical delay for acute type A dissection with malperfusion. Ann Thorac Surg 1997; 64: 1669–1675. 5. Patel HJ, Williams DM, Dasika NL, et al. Operative delay for peripheral malperfusion syndrome in acute type A aortic dissection: a long-term analysis. J Thorac Cardiovasc Surg 2008; 135: 1288–1296. 6. Yagdi T, Atay Y, Engin C, et al. Impact of organ malperfusion on mortality and morbidity in acute type A aortic dissections. J Card Surg 2006; 21: 363–369. 7. Hagan PG, Nienaber CA, Isselbacher EM, et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA 2000; 283: 897–903.
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